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BACE1-deficient (BACE1 −/−) mice have been reported initially not to show any adverse development, morphology, physiology or gross behaviour [ 11– 13].
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Diffuse unilateral subacute neuroretinitis has been reported initially in America [ 7], and later in many other countries, including China [ 8], Brazil [ 6], and India [ 9].
Src family kinases have been reported to initially phosphorylate substrates via their catalytic domain and to subsequently bind to the newly generated phosphoepitope via their SH2 domains, leading, at least in some cases, to processive phosphorylation of multiple tyrosines [ 7].
Some years ago, highly virulent systemic FCV infections associated with fatal disease have been reported in several countries, initially in North America [ 9, 10] and subsequently in Europe [ 11– 13].
Some interesting gene expression patterns with regard to sex have been reported over the past several years, initially in Drosophila melanogaster and later in other taxa (see a recent review of sex-biased gene expression by Ellegren and Parsch [ 10]).
Higher rates of serostatus change have been reported especially in cases where patients initially tested negative with the first-generation anti-JCV antibody assay and were then retested with the second-generation assay.
THA performed in Sweden have been reported to this register since 1979, initially as aggregated data based on hospital units and since 1992 as individualized data based on personal identification numbers.
Only two cases of mycotic aneurysm in patient presenting initially bacterial meningitis have been reported [ 22, 23].
It has been reported that ZAG initially appeared in urinary tract luminal surface.
It has been reported that most initially responsive patients acquire a multidrug resistance (MDR) phenotype.
Because apoptosis has been reported to occur initially following radiation in parotid salivary glands, the rate of acinar cell proliferation may provide further insight into restoration of radiation-induced tissue damage that leads to normal salivary flow rates in mice treated with post therapy IGF-1.
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